EP MICROBIOLOGY:W/DISEASES BY..-MOD.ACC
5th Edition
ISBN: 9780134607894
Author: BAUMAN
Publisher: PEARSON CO
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Chapter 10, Problem 10CT
Antiparasitic drugs in the benzimidazole family inhibit the
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We have many antimicrobial drugs to treat bacterial infections, but very few for viruses. Why is it so difficult to treat viral infections? Hint: What would the targets for the drugs be?
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a) cell to cell recognition
b) transport
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Most medically useful antibiotics interfere with either peptidoglycan synthesis or ribosome function. Why would the cell membrane be a poor target for antimicrobial medication?
Chapter 10 Solutions
EP MICROBIOLOGY:W/DISEASES BY..-MOD.ACC
Ch. 10 - Prob. 1TMWCh. 10 - Some antimicrobial drugs are harmful to humans....Ch. 10 - Antibiotic Overkill A young woman was taking...Ch. 10 - Prob. 2CCSCh. 10 - Prob. 3TMWCh. 10 - Why is it incorrect to say that an individual...Ch. 10 - Prob. 1EDCSCh. 10 - Prob. 3CCSCh. 10 - Prob. 1MCCh. 10 - In a Kirby-Bauer susceptibility test, the presence...
Ch. 10 - Prob. 3MCCh. 10 - Prob. 4MCCh. 10 - Cross resistance is _____. a. the deactivation of...Ch. 10 - Prob. 6MCCh. 10 - Prob. 7MCCh. 10 - Prob. 8MCCh. 10 - Prob. 9MCCh. 10 - Prob. 10MCCh. 10 - Label each figure below to indicate the class of...Ch. 10 - What specific test for antimicrobial efficacy is...Ch. 10 - What characteristics would an ideal...Ch. 10 - Prob. 2SACh. 10 - Why is the fact that drug Z destroys the NAM...Ch. 10 - Given that both human cells and pathogens...Ch. 10 - Prob. 5SACh. 10 - Prob. 6SACh. 10 - Prob. 7SACh. 10 - Prob. 8SACh. 10 - Compare and contrast the actions of polyenes,...Ch. 10 - Prob. 10SACh. 10 - Prob. 1CTCh. 10 - How does Penicillium escape the effects of the...Ch. 10 - How might a colony of Bacillus licheniformis...Ch. 10 - Fewer than 1 % of known antibiotics have any...Ch. 10 - In an issue of News of the Lepidopterists Society,...Ch. 10 - Even though aminoglycosides such as gentamicin can...Ch. 10 - Prob. 7CTCh. 10 - Prob. 8CTCh. 10 - Why might amphotericin B affect the kidneys more...Ch. 10 - Antiparasitic drugs in the benzimidazole family...Ch. 10 - Prob. 11CTCh. 10 - Scientists have cultured bacteria isolated from...Ch. 10 - Prob. 13CTCh. 10 - Prob. 14CTCh. 10 - Enterococcus faecium is frequently resistant to...Ch. 10 - Prob. 1CM
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- Given that both human cells and pathogens synthesize proteins at ribosomal sites, how can antimicrobial agents that target this process be safe to use in humans?arrow_forwardIt was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitation replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the…arrow_forwardIt was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitationy replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the…arrow_forward
- Identify examples of cell-wall antibiotics that are not beta-lactam drugs.arrow_forward3. The table on the last page compares for each of four different proteolytic enzymes the chemical bonding structure of a classical substrate with the structures of two competitive inhibitors. For each substrate structure an arrow indicates the position of the scissile bond, i.e., the bond that is cleaved through catalytic action. For each enzyme, one of the inhibitors is a classical competitive inhibitor while the other is a transition-state inhibitor analog. While ordinary competitive inhibitors are associated with (dissociation) inhibitor equilibrium con- stants of ~10-3 to 10-6 M, transition-state analogs exhibit inhibitor constants ≤ 10-⁹ M. (a) For each enzyme draw a circle around those parts of the substrate that account for specificity of substrate recognition. (b) For each enzyme identify the transition-state inhibitor analog by drawing a circle around it and give a brief explanation of why it mimics the structure of the transition-state species. (c) Draw a "generic"…arrow_forwardMost medically useful antibiotics interfere with either peptidoglycan synthesis or ribosome function. Why would the cytoplasmic membrane (in general) be a poor target for antibacterial medications?arrow_forward
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